Better GI Health with Mastic

Its actions on the immune system may diminish 
the systemic effects of localized inflammation

In the fields of observation, chance 
favors only the prepared mind.
— Louis Pasteur


Scientific discovery is a chancy thing. Even when opportunity presents itself and the mind is prepared through years of intensive study and hard work, there is no guarantee of success. Some scientists manage to grab the brass ring, while others miss it. Few great discoveries, in any case, occur out of nowhere, full-blown, like Botticelli’s Venus emerging from the waves. Usually they’re the culmination, by one brilliant or lucky individual, of a large body of prior work by less gifted or less fortunate scientists, some of whom may have come within a whisker of making the discovery themselves.

Perhaps they lacked some crucial bit of knowledge, yet to be discovered, that would have enabled them to complete the puzzle, or perhaps they were simply not smart enough or daring enough to make the final leap. Some, on the other hand, have been so daring in theoretical research that they became visionaries far ahead of their time, and their theories were rejected by a world ill-equipped to understand them. (For every such scientific visionary who turns out to have been right, there are a thousand crackpots, clamoring for attention, who are destined for the oblivion they deserve.)

Then there are those who really did make a tangible discovery that could readily be understood, but it went unrecognized for one reason or another, and a later rediscoverer was destined to get the credit. For an example that pertains to the subject of this article—Crohn’s disease—see the sidebar, which includes an additional story that could have come from Ripley’s “Believe It or Not.”


 Did Crohn Discover Crohn’s Disease? 

Did Macleod Deserve the Nobel Prize?

The American physician Burrill Bernard Crohn was a fine man and an outstanding gastroenterologist who was much honored during his long and productive life (he lived to age 99). One honor was having the disease that he discovered named after him. But did he really discover Crohn’s disease? Well, sort of—you’ll see.

Burrill Bernard Crohn (1884–1983)
Crohn published his first paper on the disease, which he called regional ileitis, in 1932, together with two colleagues, Leon Ginzburg and Gordon D. Oppenheimer. It was only by chance that Crohn’s name on the paper came first—the three physicians had agreed on alphabetical order for the authorship, presumably because they had shared more or less equally in the discovery. So what might otherwise have been Ginzburg’s disease or Oppenheimer’s disease—or, ideally, Crohn-Ginzburg-Oppenheimer disease (which no one wanted to have to say)—became Crohn’s disease, and Drs. G and O were shut out.


Antoni Lesniowski 
But there’s more to this story. In 1903, the Polish surgeon Antoni Lesniowski had published his first paper on regional ileitis! The world didn’t take much notice, however, perhaps because the paper appeared in a Polish journal that few outside Poland even knew about and that even fewer could read. Nonetheless, Lesniowski was the real discoverer (assuming, that is, that someone else hadn’t discovered it before he did). Thus it should rightfully be called Lesniowski’s disease. At least he does get some credit in his own country, where it’s called Lesniowski-Crohn disease.

That kind of story is by no means unique—in fact, it’s common. The history of science, technology, and medicine is replete with discoveries or inventions that were unjustly credited to someone who basically rediscovered or reinvented what some unsung hero had done previously. It’s a shame—as is the fact that many great scientists who deserved the Nobel Prize never got it, for one reason or another, and that some who didget it probably didn’t deserve it.

The story that takes the cake concerns the distinguished Canadian physiologist John Macleod, of the University of Toronto, who in 1921 was going on vacation for the summer. A new young colleague in the department, Frederick Banting, asked Macleod (his boss) if he could borrow one of his vacant laboratories for the summer, because he had a hot idea for a research project but lacked the necessary facilities; he also needed a research assistant.

Macleod agreed, with the stipulation that his name be added as coauthor to any paper that resulted from the research, and he assigned a brilliant medical student named Charles Best to assist Banting in the project. While Macleod was on vacation, Banting and Best achieved scientific immortality by discovering the role of insulin in glucose (blood sugar) regulation, thereby making diabetes a treatable disease instead of a death sentence.* The original idea was Banting’s, but Best contributed greatly to the work.

*For more on this discovery, including a photo of Banting and Best, see “Insulin Regulates Not Just Blood Sugar but Fatty Acids As Well” in the July 2002 issue.

The project was completed in 1922, by which time Macleod had taken an active interest and supervisorial role in it, but without having contributed anything but lab space—and Charles Best—to the original endeavor. The devil’s bargain stood, however, and Macleod was listed as a coauthor (which, in all fairness, he did deserve by that time).

In 1923, the Nobel committee, apparently more impressed by the esteemed professor than by the mere student, awarded the prize for this epochal discovery to Banting and Macleod! Banting was so outraged that he wanted to reject his half of the prize (which would have put Macleod in a really awkward spot), but he was persuaded to accept it. He immediately gave half of his share of the money to Best, who deserved it.

Best went on to a distinguished career in physiology. He was eventually nominated for the Nobel Prize for his later work, but again, sadly, it was not to be. Justice was twice denied.

Safety and Efficacy through Trial and Error

Let’s go back a few thousand years, to a time when our forebears were developing the practices we now call folk medicine. Their approach was not through science, of which they knew virtually nothing, but through trial and error. The lucky patients got better (or at least remained alive), while the victims of innumerable errors . . . didn’t.

For any herbal remedy that has been handed down to us through countless generations, it would be fascinating to know how long it took, in ancient times, for the idea to develop and become widely accepted that the product was both effective and safe for some ailment or other, so that one could achieve relief and not be poisoned at the same time.

Actually, safety was probably always the first to be established. One simply ate some part of the plant and waited to see whether one became sick—or dead. (Who werethose brave nutritional pioneers?) Carefully observing the dietary habits of animals was a smart strategy, but it wasn’t foolproof, because many animals can eat some things that are poisonous to humans (and vice versa). Once the safety of a plant had been established, it was only a matter of time before its medicinal efficacy, if any, would be noticed.

Who Discovered the Healing Power of Mastic?

Somewhere, at some time, there must have been a particularly perceptive person who saw a pattern that had escaped others, such as the fact that those who regularly chewed mastic, the gum resin of the mastic tree (Pistacia lentiscus, native to the Mediterranean region), had fewer gastrointestinal complaints than those who didn’t. Hmmm.

Perhaps that person—or another person with more of a flair for salesmanship—began beating the drum on behalf of mastic as a safe and effective remedy for people with tummy troubles. In so doing, he or she unknowingly bequeathed a substantial measure of gastrointestinal relief to probably millions of people, over the millennia, in the Mediterranean region—and now the world. Even if we knew who this unsung hero was, the Nobel Prize in medicine or physiology is never awarded posthumously.

In modern times, scientists have been rediscovering the health benefits that mastic offers—with the bonus of understanding, to some degree, how and why these effects occur. Most notable among mastic’s properties is its ability to kill 

Helicobacter pylori, the bacterium that causes most cases of nonerosive gastritis (a chronic inflammation of the stomach) and ulcers of the stomach or duodenum; H. pylori is also implicated in stomach cancer. Farther north in the GI tract, mastic is effective against bacterial infections of the mouth, and farther south, it’s effective against colon cancer; it may also be effective against prostate cancer and leukemia. Not bad for an ancient chewing gum!


What Is Crohn’s Disease?

One of the gastrointestinal disorders for which mastic has been found helpful is Crohn’s disease, a painful, often debilitating condition that afflicts over half a million Americans, mostly in the age range 15 to 35 (the elderly are also susceptible, however). It is one of two distinct forms of inflammatory bowel disease, the other being ulcerative colitis.

Crohn’s disease, the more severe of the two, was originally called regional ileitis because it affects primarily the terminal region of the ileum, which is the third segment (about 12 feet long) of the small intestine, before it connects with the large intestine. But because the disease can affect any region of the intestines (in fact, any region of the entire GI tract, from mouth to anus), it’s now often referred to by the broader term regional enteritis.

The disease is characterized by patchy, deeply invasive ulcers that sometimes interconnect, forming a distinctive “cobblestone” effect in the intestinal lining; there is also a narrowing and thickening of the bowel by fibrosis (the formation of fibrous tissue). The symptoms include fever, diarrhea, cramping, abdominal pain, loss of appetite, and weight loss. There is no cure, but a variety of powerful drugs can be used to alleviate the symptoms—with limited success and with unpleasant side effects.

Some Symptomatic Improvement with Mastic

In 2007, researchers in Greece published the results of a small, non-placebo-controlled pilot study showing preliminary clinical evidence for the efficacy of mastic against Crohn’s disease (CD).1 The subjects were 18 men and women—10 patients with mild to moderate CD and 8 healthy controls—all of whom received 2.2 g of mastic powder daily for 4 weeks.*

The CD patients showed some symptomatic improvement, and there were significant reductions in their plasma levels of two of the four biochemical markers of inflammation that were measured. In addition, they experienced a large increase in their “total antioxidant potential,” a measure of the body’s ability to combat oxidative stress, which is associated with inflammatory processes.

How Does Mastic Affect the Inflammation?

Now the Greek researchers have published a follow-up paper derived from the same study, this time discussing the results of a different set of measurements made on cells from the patients’ blood.2 (Such splitting of the results is one way to make your list of publications look more impressive to the academic review committee.)

In the new paper, they focused on mastic’s effect on four cytokines, which are biochemical markers of inflammation: interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1), and macrophage migration-inhibitory factor (MIF), the first three of which were discussed in the authors’ previous paper.* Here, however, the interest was not in the plasma levels of these substances, but rather in their levels in the patients’ peripheral blood mononuclear cells (PBMCs).

*Cytokines act as regulators of the immune system and as cell-to-cell messenger molecules. Most are proinflammatory, but some are anti-inflammatory. There are about 40 different kinds, interacting in complex and subtle ways as a “cytokine network.”

Mononuclear cells, or monocytes, are a type of white blood cell that plays an important role in the immune system. When monocytes leave the blood circulation and enter the tissues in response to some infection or injury, they become macrophages, a type of large scavenger cell that devours bacteria, foreign cells, and damaged or dead cells. So monocytes and macrophages are two sides of the same coin. The standard definition of MIF as macrophage migration-inhibitory factor also applies to monocytes. In either case, the effect of MIF is, as its name implies, to prevent the cell from migrating to other locations in the body.

Freeze, Monocytes!

In the acute inflammatory process of Crohn’s disease, monocytes become “activated” and produce excessive amounts of certain proinflammatory cytokines—but not of MIF. That implies a relative lack of migratory inhibition, and if the activated monocytes were not inhibited from migrating, they could travel to other tissues throughout the body via the peripheral blood. This, the researchers hypothesized, might explain how the localized inflammation in the GI tract in CD produces systemic effects. Hence their interest in the levels of cytokines—especially MIF—in the PBMCs.

What they found was that the levels of MIF in the CD patients’ PBMCs were initially (at baseline) lower than those in the healthy controls. In the patients (but not the controls), they increased significantly with mastic treatment. That’s good, because this would tend to keep the activated monocytes, and hence the inflammation, more localized and their effects less systemic.

A Proinflammatory Cytokine Is Reduced

The researchers also found that the levels of TNF-α in the PBMCs were initially no different between the patients and controls, and in the patients (but not the controls), they were significantly reduced by mastic.* That’s good, because TNF-α is a proinflammatory cytokine. (Even though MIF has been characterized as a proinflammatory cytokine in other studies, the authors stated that it appeared not to have acted in that manner in this study.)

*In the plasma, TNF-α was initially much higher in the CD patients than in the controls, which suggests that the excess came from sources other than PBMCs.

The levels of IL-6 and MCP-1 were unaffected by mastic. Also unaffected, despite the increases in the patients’ total antioxidant potential (TAP), were the levels of the important antioxidant glutathione. Thus the rise in TAP was presumably due to mastic’s effects on other antioxidants. (Mastic is known to increase glutathione levels in cell cultures; it’s not uncommon, however, for the effects seen in laboratory experiments to fail to materialize in living beings.)

Thank You, ______________

Whether mastic turns out to be an effective treatment for Crohn’s disease remains to be seen, but the signs are promising. Also promising—not just for Crohn’s disease but also for the other (less severe) inflammatory bowel disease, ulcerative colitis—are the nutrients fish oil and vitamins C and E.3 Fish oil contains high levels of the omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), which can help tip the patients’ immune system toward a lower level of inflammation. The vitamins can help boost the patients’ total antioxidant potential. Thus far, however, none of these nutrients has been found to reduce the actual disease activity in the patients studied.

So, for inflammatory bowel disease, we must await further discoveries—but when or from where they will come, we know not. Meanwhile, we do know that mastic has earned its place in the pantheon of time-tested nutritional supplements because of its beneficial effects on a variety of gastrointestinal ailments.* If only we knew whom to thank (very posthumously) for that discovery.


  1. Kaliora AC, Stathopoulou MG, Triantafillidis JK, Dedoussis GVZ, Andrikopoulos NK. Chios mastic treatment of patients with active Crohn’s disease. World J Gastroenterol 2007;13(5):748-53.
  2. Kaliora AC, Stathopoulou MG, Triantafillidis JK, Dedoussis GVZ, Andrikopoulos NK. Alterations in the function of circulating mononuclear cells derived from patients with Crohn’s disease treated with mastic. World J Gastroenterol 2007;13(45):6031-6.
  3. Razack R, Seidner DL. Nutrition in inflammatory bowel disease. Curr Opin Gastroenterol 2007;23:400-5.